Interpretive Summary: The control of the southern cattle tick, Boophilus microplus, in Mexico continues to rely on chemical acaricides. Resistance to all major classes of acaricide, including organophosphates, pyrethroids and amitraz, in Mexican tick populations in recent years poses a major threat to the USDA’s Cattle Fever Tick Eradication Program. In order to develop an effective resistance management strategy, a study was conducted by a research team at the USDA, ARS, Knipling-Bushland Livestock Insects Research Laboratory in Texas to examine the mechanisms and genetic basis of permethrin resistance in a resistant strain of B microplus. This study investigated the mechanisms of resistance using a larval packet bioassay and biochemical assay method. The data suggest a possible new mechanism of resistance to permethrin in this Brazilian tick strain. The results from this study also indicate that resistance to permethrin is controlled by a single major recessive gene. As this gene is linked to the gene that is involved in amitraz resistance, selection with either permethrin or amitraz would lead to increase of resistance to both acaricides. Data collected from this study have significant implications in resistance management that may prolong the useful life of the acaricides that are currently employed for tick and control and eradication in Mexico and the United States.

Technical Abstract:
A study was conducted at the USDA Cattle Fever Tick Research Laboratory in Texas to investigate the genetic basis of permethrin resistance with cross-mating experiments, and to determine the mechanisms of permethrin resistance through synergist bioassays and biochemical analysis of esterase profiles. The Munoz strain, an acaricide-susceptible reference strain, was used as the susceptible parent and the Santa Luiza strain, originating in Brazil, was used as the resistant parent. The FAO Larval Packet Test was used to estimate the degrees of susceptibility of larvae of the parental strains, F1, backcross, F2, and F3 generations to permethrin. Results of reciprocal crossing experiments suggested that permethrin resistance was inherited as an incomplete recessive trait. There was no significant maternal effect on larval progeny’s susceptibility to permethrin in the F1 and subsequent generations. The values of the degree of dominance were estimated at – 0.700 and – 0.522 for the F1 larvae with resistant and susceptible female parents, respectively. Results of bioassays on larval progeny of the F1 backcrossed with the resistant parent strain and of the F2 generations suggested that one major gene was responsible for permethrin resistance in the Santa Luiza strain. Selection of F3 larvae with either permethrin or amitraz led to significantly increased resistance to both permethrin and amitraz, indicating a close linkage between genes responsible for permethrin and amitraz resistance. The possible involvement of metabolic enzymes in permethrin resistance in the Santa Luiza strain of B. microplus was dismissed by the lack of enhanced synergism by TPP or PBO, as observed in synergist bioassays, as well as by the lack of enhanced esterase activity in the Santa Luiza strain relative to the susceptible strain. The results of this study suggest that other mechanisms, including a possible new sodium channel mutation that is different from the one currently known, may be responsible for permethrin resistance in the Santa Luiza strain of B. microplus.